Iatrogenic complications of Steroid Treatments Flashcards Preview

Gabe's Endocrinology > Iatrogenic complications of Steroid Treatments > Flashcards

Flashcards in Iatrogenic complications of Steroid Treatments Deck (38)
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1

What does the amount of drug bound to a carrier protein depend on?

Affinity and the relative concentrations of drug and protein

2

What is the general binding protein in the serum?

Albumin is a general binding protein, but specific proteins exist for several hormones (e.g. thyroxin binding globulin)

3

What binds thyroxin in the plasma?

Thyroxin binding globulin (TBG)

4

When does thyroxine (T4) mostly act?

After conversion to T3

5

Where is 99.96% of thyroxine protein?

Bound in the plasma (mostly to thyroxine binding globulin)

6

What is the volume of distribution of thyroxine?

10L

7

What is the half life of Thyroxine (T4)?

~7 days

8

Which is more active, Liothyronine (T3) or Thyroxine (T4)?

Liothyronine (T3)

9

Which is more strongly bound to its carrier protein, T3 or T4?

T4 is more strongly bound

10

What is the half-life of T3?

~1 day

11

Which has more stable levels during the day, T3 or T4?

T4

12

Are TSH levels easily interpreted in patients taking T3?

No

13

When is Liothyronine (T3) used as a therapeutic instead of T4?

When treating severe hypothyroid and myxoedema coma. For most patients, use T4 rather than T3.

14

What is the interplay between T3 and cortisol?

Cortisol inhibits conversion of T4 to T3 and T3 inhibits cortisol production.

15

When do cortisol levels peak in the diurnal cycle?

In the morning, between 8-9am.

16

When are cortisol levels at their lowest?

Between midnight and 1am.

17

What happens to cortisone at the liver?

It is converted to cortisol

18

What happens to cortisol at the kidney?

It is converted to cortisone

19

What is the difference between cortisone and cortisol?

Cortisone is inactive at the mineralocorticoid receptor, whereas cortisol is active.

20

Which enzyme is responsible for converting cortisone to cortisol in the liver?

11β-HSD-1

21

Which enzyme is responsible for converting corisol to cortisone in the kidney?

11β-HSD-2

22

What can be used as an in vivo assay for analysis of human 11β-HSD2 activity?

11α-deuterium cortisol

23

What does cortisol deficiency present with?

Weakness, fatigue, anorexia, nausea, vomiting, hypotension and hypoglycaemia.

24

Why is the hyperkalaemia, hyponatraemia, acidosis and dehydration in adrenal hypofunction?

Because cortisol deficiency is combined with mineralocorticoid deficiency to cause hyperkalaemia and hyponatraemia, acidosis and dehydration.

25

What is used to treat cortisol deficiency?

Cortisol (hydrocortisone) or cortisone

26

What is done to the cortisol dosage in cortisol deficiency?

The dose is divided to mimic the physiological timecourse.

27

What is oral cortisone's bioavailability compared to cortisol?

Slightly less (25mg cortisone = 20mg cortisol)

28

What are some iatrogenic complications of glucocorticoid therapy?

  • Cushingoid syndrome
  • Adrenal suppression
  • Immunosuppression (reactivation of latent tuberculosis)
  • Peptic ulcers
  • Osteoporosis
  • Inhibition of linear growth in children

29

What is the major complication of glucocorticoid therapy?

Adrenal suppression

30

How can adrenal suppression in glucocorticoid therapy be minimised?

  • Allow for ACTH secretion if possible
  • Avoid long-lasting drugs
  • Alternate day dosing
  • Morning dosing
  • Minimise systemic absorption of steroids
  • Inhaled or topical (but note: still absorbed!)
  • Third generation glucocorticoid drug